Eating epilepsy associated with a deep forebrain glioma.

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Eating Epilepsy
Associated with a
Deep Forebrain Glioma
W. C. Robertson, Jr, MD,
and R. G. Fariello, MD
Seizures associated with deglutition are rare, and previously reported cases of so-called eating epilepsy have
not identified specific electrophysiological or anatomical foci. We evaluated a 14-year-old with a deep hemispheric astrocytoma in whom focal seizures were consistently triggered by eating. Electroencephalograms
were consistent with a deeply located seizure focus.
Eating epilepsy should be grouped with reflex epilepsies that may originate with the diencephalon.
Robertson WC Jr, Fariello RG: Eating epilepsy
associated with a deep forebrain glioma. Ann
Neurol 6:271-273, 1979
Seizures associated with eating, or so-called eating
epilepsy, are extremely rare. Recently we evaluated a
14-year-old with an astrocytoma of the basal ganglia
and focal seizures consistently triggered by eating.
Two weeks earlier, a 14-year-old boy had developed the
first of three episodes characterized by numbness of the left
side of the face followed by clonic movements of left facial
muscles. The spells lasted 1 to 2 minutes and were not
associated with altered consciousness. The clinical examination was normal. Laboratory studies, including computerized tomography, radionuclide brain scan, and cerebral angiography, were negative. An electroencephalogram
demonstrated focal slowing in the right frontotemporal
area. He was treated with phenytoin and phenobarbital.
Three months later he began to have spells consisting of
paresthesias of the left side of the face followed by numbness and tingling of the left hand and arm and then by
clonic movements of the left facial muscles. These spells
lasted for 1 to 2 minutes, were not associated with disturbed consciousness, and were invariably produced by
eating. The boy became reluctant to eat even though, after
having one spell, he could complete the remainder of a
meal without having seizures recur.
The spells were not produced by masticatory movements
or swallowing. Pressure on the gums, teeth, tongue, or
buccal mucosa did not elicit a seizure. However, chewing
food or holding liquids within the mouth consistently re-
From the Department of Neurology, University of Wisconsin
Clinical Sciences Center, Madison, WI.
Accepted for publication Apr 15, 1979.
Address reprint requests to Dr Fariello, University Hospitals
Clinical Science Center, 600 Highland Ave, H 4 621, Madison, WI
53792.
sulted in one of the previously described spells. Once a
spell occurred, another seizure could not be produced for
20 to 30 minutes. EEG studies disclosed a delta focus over
the right frontal region. In subsequent recordings, occasional spikes and sharp waves were seen in the same area.
After the oral cavity was anesthetized with viscous
lidocaine, a meal was served during a prolonged EEG recording. Despite effective anesthesia of the oral cavity, a
typical seizure was produced, characterized by a rhythmic
theta discharge followed by sharp-wave and spike activity
over the right frontal region (Fig 1). During the second
hospitalization the patient also began to experience spells
unassociated with eating.
CT scanning demonstrated a mass in the region of the
anterior limb of the internal capsule (Fig 2) with involvement of the head of the right caudate nucelus. The patient
underwent a frontal craniotomy with subtotal resection of a
low-grade astrocytoma. He has since been maintained on
phenobarbital, dilantin, and dexamethasone. During the
four months following surgery there were no seizures.
Discussion
Disturbance of consciousness associated with deglutition is usually secondary to syncope from a vasovagal
reflex [ 111. Although masticatory movements, salivation, and gustatory sensations may be part of partial
complex seizures [ 5 ] , the production of these
symptoms from eating is rare. We are aware of only 3
previous cases of so-called eating epilepsy [2, 71. In
all instances, eating food produced clinical and EEG
evidence of a seizure. Patients did not lose consciousness, but during attacks they were unable to
speak. One of Forster’s patients [27 was studied extensively and did not appear to have seizures from
actual sensory stimulation of the oral cavity. EEGs
showed an interictal right temporal focus and a generalized cortical electrodecremental event during seizures, with total suppression of the interictal spiking
[ 13. Because Forster’s patient underwent prolonged
EEG recordings with videotaping, we had the opportunity to review the original data. In that patient,
as in the present case, the production of seizures was
independent of the taste, quality, quantity, or other
physical characteristics of ingested food o r liquid. In
both patients, anesthesia of the oral cavity did not
prevent seizures. These observations and the fact that
seizures did not occur when the patients were asked
to chew o r swallow in the absence of food suggest
that specific elementary sensory mechanisms arising
from the oral cavity did not act as determinant triggers.
We believe that the triggering mechanism in these
eating-related fits may result from activation of
hypothalamic nuclei, which are the diencephalic
structures involved in the cephalic phase of digestion.
Supporting this hypothesis is the observation by
Scollo Lavizzari and Hess [7] that their patient’s
0364-5134/79/090271-04$01.25 @ 1978 by Ruggero G. Fariello 271
F i g 2.Preoperatiz'r CT .si-un.rshowin,q a muss with ini.rrased
densit? deep in the right henii.rpherr. The anterior limb ojthe
internal i-upsuleand the right i audate nut-ku.i are inz'olved.
The headof the right 1-audatenurleus bulgi,s into thr right
lateral ventricle and almost obliteratrs it.
F i g 1 . E E G vet-ordedduring an eatiwg-iwduirdsrizure. (A)
During the Left s e n j o r j aura. build-up of a rh)thtnii-theta is
mw oii electrodes F , and C4. (Interz~alof j 5 w o r d s btal ~ P I ZA
and B . ) (B) During the jaiksoniun .\eizurc (see regular mustle
a r t i f a t on the leji temporal leads) the srizure discharge spreads
t o the intire right hemisphere. i l n t e r ~ ~oj
a l 100 3.eionds brtii eeii
B and C . ) ICI When the behavioral/Zt i.r tcrmiwated, a rtpetititme sharp ii,atse is still abserzed in the right frontal leads at
rler-trode F,.
272
Annals of Neurology
Vol 6 No 3
September 1979
spells were elicited not only by actual eating, but in
some instances also by simple presentation of food.
The ictal EEG of Forster’s patient suggested a deeply
located focus rather than a cortical one [ 11, and in our
own patient the electrographically recorded seizures
did not show the characteristic recruiting discharge
typically seen in spells of purely cortical origin [3, 61.
In addition, the EEG findings in our patient are similar to the abnormalities observed interictally and ictally in other patients with deep hemispheric lesions.
Indeed, the presence of an electroencephalographically detectable spike does not preclude the existence
of a subcortical lesion. Sterotaxic exploration with
depth electrodes in candidates for temporal lobectomy has shown that the cortical EEG is at times a
poor indicator of the complex pathophysiology of
partial complex seizures [4].Thus, the cortical discharge often does not reflect the actual site of origin
of the paroxysmal activity that starts the ictal event.
Our observations suggest that eating epilepsy should
be grouped with other types of reflex epilepsy that
may originate within the diencephalon, such as hot
water epilepsy [9] and emotional epilepsies IS, lo].
Prof F. M. Forster generously made available the original material
o n his patient with eating epilepsy.
References
1. Fariello RG, Doro JM, Forster FM: Generalized electrodecremental event. Clinical and neurophysiological observations in patients with dystonic seizures. Arch Neurol
36:285-291, 1979
2. Forster FM: Reflex Epilepsy: Behaviour Therapy and Conditional Reflexes. Springfield, IL, Thomas, 1977, pp 156-163
3. Geiger LR, Harner RN: EEG patterns at the time of focal
seizure onset. Arch Neurol 35:276-286, 1978
4. Lieb JP, Walsh GO, Babb TL, et al: A comparison of EEG
seizure patterns recorded with surface and depth electrodes in
patients with temporal lobe epilepsy. Epilepsia 17:137-160,
1976
5. Penfield W, Jasper H : Epilepsy and the Functional Anatomy
of the Human Brain. Boston, Little, Brown, 1954, p 896
6. Ralston BL, Papatheodorou CA: The mechanism of transition
of interictal spiking foci into ictal seizure discharges. Part 11:
Observations in man. Electroencephalogr Clin Neurophysiol
12:297-306, 1960
7. Scollo Lavizzari G , Hess R: Sensory precipitation of epileptic
seizures-report on two unusual cases. Epilepsia 8:157-161,
1967
8. Servit 2: Application of reflex theory in the interpretation of
the clinical picture of epilepsy, in Servit 2 (ed): Reflex Mechanisms in the Genesis of Epilepsy. Amsterdam, Elsevier,
1963, p 107
9. Simonowitz W, Melloff KL: Hot water epilepsy. Can J Neurol
Sci 5:247-251, 1978
10. Stevens J: Emotional activation of the EEG in patients with
convulsive disorders. Electroencephalogr Clin Neurophysiol
10:177-178, 1958
11. Weiss S, Ferris EB Jr: Adams-Stokes syndrome with transient
complete heart block of vagovagal reflex origin. Mechanism
and treatment. Arch Intern Med 56931-938, 1934
Case Report: Robertson and Fariello: Eating Epilepsy 273